BOWIE, PUROHIT, ADAMS, SOMAIAH, HAWTHORNE AND HINDS 549 
Table VI. — Effect of Glucagon Infusion on Cardiovascular Measurements in a Chronic Horse {10 mg) 
End- Cardiac Ejection Left 
Time 
Min Sec 
Diastolic 
Volume (ml) 
End-systolic 
Volume (ml) 
Stroke 
Volume (ml) 
Heart Rate 
(beats/min) 
Output 
(L/min) 
Fraction 
(% EDV) 
Stroke work 
( Gm-meters ) 
Ventricular 
Pressure 
Aortic 
Pressure 
PSP 
PSP 
0 
957 9 
490.9 
467.0 
90 
42.0 
48.8 
508.1 
124 
108 
1 
1031. G 
445.9 
585.7 
102 
59.7 
56.7 
647.8 
120 
104 
2 
1031.6 
404.1 
627.5 
107 
67.1 
60.8 
716.8 
124 
108 
2 
30 
1031.6 
445.9 
585.7 
111 
65.0 
56.7 
669.1 
128 
112 
2 
45 
1031.6 
404.1 
627.5 
108 
67.7 
60.8 
705.5 
128 
118 
3 
1031.6 
445.9 
585.7 
108 
61.5 
56.7 
690.3 
124 
108 
4 
957.9 
404.1 
627.5 
105 
58.1 
57.8 
582.4 
120 
100 
5 
957.9 
449.9 
508.0 
106 
53.8 
53.0 
534.0 
120 
96 
7 
1031.6 
445.9 
585.7 
105 
61.5 
56.7 
690.3 
128 
108 
8 
1031.6 
490.5 
541.1 
102 
55.1 
52.4 
773.4 
132 
118 
9 
1190.0 
537.8 
652.1 
94 
61.3 
54.7 
827.7 
138 
124 
10 
957.9 
445.9 
512.0 
97 
49.6 
53.4 
547.7 
120 
104 
11 
957.9 
445.9 
512.0 
100 
51.2 
53.4 
570.9 
126 
104 
12 
1108.9 
490. 
618.0 
97 
59.9 
55.7 
706. 
128 
104 
15 
957.9 
445.9 
512.0 
95 
48.5 
53.4 
529.2 
116 
84 
cardiovascular response reached a peak 2 to 3 
minutes later and was followed by a gradual de- 
crease in activity. There was not a complete re- 
turn to the control values after 15-20 minutes. 
The effect of glucagon infusions on the hemo- 
dynamic system of the horse appears to be more 
akin to those reported in man^" than to the re- 
sponses found in dogs. These effects are charac- 
terized by an increase in the cardiac output re- 
sulting equally from elevations in heart rate 
and stroke volume. In dogs, the increase in car- 
diac output is due entirely to tachycardia.^^ 
SUMMARY 
The technique used for dimensional measure- 
ments allowed us to calculate left ventricular in- 
ternal volumes during continuous cardiac cy- 
cles. Along with measurements of change in 
internal diameter from end-diastolic to end-sys- 
tolic size, ventricular and aortic pressures were 
also measured. These measurements permitted 
us to make the following determinations: left 
ventricular internal end-diastolic volume, end- 
systolic volume, stroke volume, cardiac output, 
ejection fraction, and stroke work. 
Studies with anesthestized and conscious 
horses showed that there was a marked effect of 
anesthesia on the cardiovascular values. Pento- 
barbital and halothane caused a 50% reduction 
in the cardiac output. 
Rapid intravenous infusion of Tyrode's solu- 
tion caused an increase in end-diastolic volume, 
end-systolic volume, stroke volume, stroke 
work, and the cardiac output. The increase in 
cardiac output was mainly due to the increased 
stroke volume since the heart rate was not 
changed. The elevation in stroke volume ob- 
tained by the volume overload was primarily 
due to the increase in the end-diastolic size of 
the left ventricle. 
Isoproterenol and epinephrine produced simi- 
lar directional changes in cardiovascular data 
of the equine heart. The effects of norepineph- 
rine differed markedly from those of epineph- 
rine and isoproterenol. Isoproterenol and epi- 
nephrine caused an increase in heart rate and 
cardiac output, and a decrease in end-diastolic 
and end-systolic volume, with a generally varia- 
ble or unchanged stroke volume and stroke 
work. Norepinephrine caused a slight decrease 
in end-diastolic volume and end-systolic volume, 
unchanged or slightly variable heart rates, vir- 
tually unchanged cardiac output, variable or un- 
changed stroke volume and ejection fractions, 
and a marked increase in stroke work. 
Intravenous administration of glucagon re- 
sulted in increased left ventricular end-diastolic 
volume, increased stroke volume, increased 
heart rate, and increased stroke work. In- 
creased cardiac output was the result of both an 
increase in stroke volume and heart rate. This 
is in contrast to the response to epinephrine and 
isoproterenol where the increased cardiac out- 
put was the result of an increasing heart rate, 
but not an increasing stroke volume. 
The cardiovascular effects of glucagon are 
similar in some respects to those of beta reac- 
tive catecholamines, these effects being both 
